1,721,067 research outputs found
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Variations on the Author
Full text link“Variations on the Author” discusses two of Eduardo Coutinho’s recent films (Um Dia na Vida, from 2010, and Últimas Conversas, posthumously released in 2015) and their contribution to the general question of documentary authorship. The director’s filmography is characterized by a consistent yet self-effacing form of authorial self-inscription: Coutinho often features as an interviewer that rather than express opinions propels discourses; an interviewer that is good at listening. This mode of self-inscription characterizes him as an author who is not expressive but who is nonetheless markedly present on the screen. In Um Dia na Vida, however, Coutinho is completely absent form the image, while Últimas Conversas, on the contrary, includes a confessional prologue that moves the director from the margins to the center of his films. This article examines the ways in which these works stand out in the filmography of a director who offers new insights into the notion of cinematic authorship
Appropriate Similarity Measures for Author Cocitation Analysis
Full text linkWe provide a number of new insights into the methodological discussion about author cocitation analysis. We first argue that the use of the Pearson correlation for measuring the similarity between authors’ cocitation profiles is not very satisfactory. We then discuss what kind of similarity measures may be used as an alternative to the Pearson correlation. We consider three similarity measures in particular. One is the well-known cosine. The other two similarity measures have not been used before in the bibliometric literature. Finally, we show by means of an example that our findings have a high practical relevance.information science;Pearson correlation;cosine;similarity measure;author cocitation analysis
Dispelling the Myths Behind First-author Citation Counts
Full text linkWe conducted a full-scale evaluative citation analysis study of scholars in the XML research field to explore just how different from each other author rankings resulting from different citation counting methods actually are, and to demonstrate the capability of emerging data and tools on the Web in supporting more realistic citation counting methods. Our results contest some common arguments for the continued
use of first-author citation counts in the evaluation of scholars, such as high correlations between author rankings by first-author citation counts and other citation
counting methods, and high costs of using more realistic citation counting methods that are not well-supported by the ISI databases. It is argued that increasingly available digital full text research papers make it possible for citation analysis studies to go beyond what the ISI databases have directly supported and to employ more
sophisticated methods
Fundamentals of the Host-Virus Evolutionary Arms Race
Full text linkThesis (Ph.D.)--University of Washington, 2012The immune system has been battling viral infections over the course of millions of years in primate evolution. The constant evolution of hosts and viruses to defeat the other has led to a high stakes genetic arms race. Here I present a detailed study of three antiviral proteins locked in antagonistic viral conflict called Tetherin, Viperin and SAMHD1. Using a combined approach of virology and evolutionary biology, I have reconstructed their evolutionary arms race between primates and lentiviruses, including HIV-1, HIV-2 and related SIVs. The broad themes that emerge from my research are two-fold. First, lentiviruses are able to evolve new functions within existing gene repertoires to counteract rapidly evolving host antiviral genes. Second, hosts escape from viral pressure either by single amino acid changes or by deletions of a `susceptibility domain'. Thus, my thesis research has helped define the rules by which host-virus arms races ensue. Based on my findings, we contend that the host evolutionary framework is a fundamental pillar of antiviral restriction
Virus-driven evolution of an antiviral gene in deep and shallow time
No full textThesis (Ph.D.)--University of Washington, 2012The emergence of AIDS in the early 20th century has provoked studies to better understand the evolutionary history of viruses and the factors that govern their spread. Pandemic Human Immunodeficiency Virus-type 1 (HIV-1), which currently infects 34 million people worldwide, emerged following the transmission of a lentivirus between chimpanzees and humans. A growing list of apparently nonpathogenic, species-specific simian strains (known as Simian Immunodeficiency Virus) has now been characterized in dozens of African primates, suggesting that primate lentiviruses are older and more widespread than originally thought. To estimate the extent to which primates and lentiviruses have coexisted, and to determine whether past and present lentivirus infections exhibit pathogenesis, we tracked the interaction between host and virus on a molecular level over evolutionary time. Specifically, we characterized the lentivirus-driven evolution of host restriction factor APOBEC3G (A3G) in Old World Monkey (OWM) species. We found that residues 128 and 130 of A3G, which determine susceptibility to antagonism by the lentiviral accessory protein Vif, are undergoing recurrent adaptive evolution in both ancestral and contemporary primate populations. We used a broad panel of SIV Vif isolates to demonstrate that natural variation in OWM A3G confers resistance to Vif-mediated degradation, suggesting that adaptive variants of the host factor were selected upon exposure to pathogenic lentiviruses at least 5-6 million years ago (MYA). Furthermore, in members of the divergent Colobinae subfamily of OWM, a multi-residue insertion event in A3G that arose approximately 12 MYA blocks the activity of Vif, suggesting an even more ancient origin of SIV. In response to these two adaptive strategies employed by OWM hosts, Vif proteins have counter-evolved to target distinct surfaces of the A3G substrate. Furthermore, some Vif proteins, like that of SIVsm infecting sooty mangabeys, have evolved broad specificity that may facilitate cross-species transmission events. Our findings support that a genetic conflict between primates and lentiviruses has been underway for millions of years and continues to this day. The ancient and ongoing conflict we described may have important implications for our understanding of HIV pathogenesis and spread in human populations. Our studies reveal that, while primate lentiviruses may have modern consequences for human health, they have ancient origins in our non-human primate relatives
koamabayili/VECTRON-author-checklist: VECTRON author checklist
No full textWe have done our best to complete the author checklist relating to the use of animals in the hut study. Note that the objective for the hut study was to evaluate the IRS treatment applications for residual efficacy against Anopheles mosquitoes, including the local An. coluzzii mosquito population. Cows were only used to attract mosquitoes into the huts and no tests were carried out directly on the cows. The author checklist is intended for use with studies where experiments are carried out on animals, which is why we have had such difficulty in completing this for the hut study, as many of the questions do not relate to how the cows were used
TRIM34 and TRIM5a co-operatively restrict primate lentiviruses
Full text linkThesis (Ph.D.)--University of Washington, 2023Human immunodeficiency virus (HIV) and other lentiviruses adapt to new hosts by evolving to evade host-specific innate immune proteins that differ in sequence and often viral recognition between host species. Understanding how these host antiviral proteins, called restriction factors, constrain lentivirus replication and transmission is key to understanding the emergence of pandemic viruses like HIV-1. One such restriction factor is TRIM5α, which blocks replication by multimerizing onto the HIV core, inducing aberrant capsid uncoating. TRIM5α-mediated restriction requires multimerization of TRIM5α monomers. Human TRIM34, a paralogue of the well-characterized lentiviral restriction factor TRIM5α, was previously identified by our lab via CRISPR-Cas9 screening as a restriction factor of certain HIV and SIV capsids. Notably, TRIM34-mediated restriction requires TRIM5α. Thus, we propose that TRIM34 requires multimerization with TRIM5α to restrict lentiviral capsids. Here, we show that diverse primate TRIM34 orthologues from non-human primates can restrict a range of Simian Immunodeficiency Virus (SIV) capsids including SIVAGM-SAB, SIVAGM-TAN and SIVMAC capsids, which infect sabaeus monkeys, tantalus monkeys, and rhesus macaques, respectively. All primate TRIM34 orthologues tested, regardless of species of origin, were able to restrict this same subset of viral capsids. We demonstrate that TRIM5α is necessary, but not sufficient, for TRIM34-mediated restriction of these capsids, and that human TRIM5α functionally interacts with TRIM34 from different species. Finally, we find that both the TRIM5α SPRY domain, in particular the v1 loop, and the TRIM34 SPRY domain are essential for TRIM34-mediated restriction.
These data suggest that TRIM34 is a conserved primate lentiviral restriction factor and that TRIM34 and TRIM5α interact with each other and capsids. This supports a model in which TRIM34 is a broadly conserved primate lentiviral restriction factor that acts in tandem with TRIM5α, such that together, these proteins can restrict capsids that neither can restrict alone. The goals of this work are to define the range of primate lentiviruses against which TRIM34 is active, identify determinants of antiviral specificity for TRIM34-mediated restriction, to identify domains of TRIM34 and TRIM5α that are required for lentiviral restriction. Ultimately, these studies can help lead to a better understanding of TRIM34’s role in host-pathogen evolutionary history
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